ArticleBritish journal of pharmacology2011
cAMP inhibits modulation of airway smooth muscle phenotype via the exchange protein activated by cAMP (Epac) and protein kinase A.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Pharmacological inhibition of Epac1 protects against pulmonary fibrosis by blocking FoxO3a neddylation.The European respiratory journal · 2025Article
- βLung · 2021Article
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Disruption of AKAP-PKA Interaction Induces Hypercontractility With Concomitant Increase in Proliferation Markers in Human Airway Smooth Muscle.Frontiers in cell and developmental biology · 2020Article
- Exchange protein directly activated by cAMP (Epac) protects against airway inflammation and airway remodeling in asthmatic mice.Respiratory research · 2019Article
- Review
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- Epac1 interacts with importin β1 and controls neurite outgrowth independently of cAMP and Rap1.Scientific reports · 2016Article
- Differential impact of acute and prolonged cAMP agonist exposure on protein kinase A activation and human myometrium contractile activity.The Journal of physiology · 2016Article
- Article
- A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.British journal of pharmacology · 2014Review
- β-Agonist-mediated relaxation of airway smooth muscle is protein kinase A-dependent.The Journal of biological chemistry · 2014Article
- Clonally expanded human airway smooth muscle cells exhibit morphological and functional heterogeneity.Respiratory research · 2014Article
- The cAMP effector EPAC activates Elk1 transcription factor in prostate smooth muscle, and is a minor regulator of α1-adrenergic contraction.Journal of biomedical science · 2013Article
- cAMP regulation of airway smooth muscle function.Pulmonary pharmacology & therapeutics · 2013Review
- Multiple facets of cAMP signalling and physiological impact: cAMP compartmentalization in the lung.Pharmaceuticals (Basel, Switzerland) · 2012Article
- Cyclic AMP signaling inhibits megakaryocytic differentiation by targeting transcription factor 3 (E2A) cyclin-dependent kinase inhibitor 1A (CDKN1A) transcriptional axis.The Journal of biological chemistry · 2012Article
- Anti-inflammatory role of the cAMP effectors Epac and PKA: implications in chronic obstructive pulmonary disease.PloS one · 2012Article
- Protein kinase A and the exchange protein directly activated by cAMP (Epac) modulate phenotype plasticity in human airway smooth muscle.British journal of pharmacology · 2011Article
- Beyond phosphorylation: nuclear export in vascular remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeChanges in airway smooth muscle (ASM) phenotype may contribute to the pathogenesis of airway disease. Platelet-derived growth factor (PDGF) switches ASM from a contractile to a proliferative, hypo-contractile phenotype, a process requiring activation of extracellular signal-regulated kinase (ERK) and p70(S6) Kinase (p70(S6K) ). The effects of cAMP-elevating agents on these processes is unknown. Here, we investigated the effects of cAMP elevation by prostaglandin E(2) (PGE(2) ) and the activation of the cAMP effectors, protein kinase A (PKA) and exchange protein activated by cAMP (Epac) on PDGF-induced phenotype switching in bovine tracheal smooth muscle (BTSM). EXPERIMENTAL APPROACH: Effects of long-term treatment with the PGE(2) analogue 16,16-dimethyl-PGE(2) , the selective Epac activator, 8-pCPT-2'-O-Me-cAMP and the selective PKA activator, 6-Bnz-cAMP were assessed on the induction of a hypo-contractile, proliferative BTSM phenotype and on activation of ERK and p70(S6K) , both induced by PDGF. KEY
resultsTreatment with 16,16-dimethyl-PGE(2) inhibited PDGF-induced proliferation of BTSM cells and maintained BTSM strip contractility and contractile protein expression in the presence of PDGF. Activation of both Epac and PKA similarly prevented PDGF-induced phenotype switching and PDGF-induced activation of ERK. Interestingly, only PKA activation resulted in inhibition of PDGF-induced phosphorylation of p70(S6K) . CONCLUSIONS AND IMPLICATIONS: Our data indicate for the first time that both Epac and PKA regulated switching of ASM phenotype via differential inhibition of ERK and p70(S6K) pathways. These findings suggest that cAMP elevation may be beneficial in the treatment of long-term changes in airway disease.
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